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Series GSE63717 Query DataSets for GSE63717
Status Public on Jun 03, 2015
Title Condensin-Driven Remodeling of X-Chromosome Topology during Dosage Compensation [Hi-C]
Organism Caenorhabditis elegans
Experiment type Other
Summary The three-dimensional (3D) organization of a genome plays a critical role in regulating gene expression, yet little is known about the machinery and mechanisms that determine higher-order chromosome structure or how structure influences gene expression. Here we exploit the X-chromosome-wide process of dosage compensation to dissect these mechanisms. The dosage compensation complex (DCC) of C. elegans, a condensin complex, binds to both X chromosomes of hermaphrodites via sequence-specific recruitment sites (rex sites) to reduce chromosome-wide gene expression by half. Using genome-wide chromosome conformation capture and single-cell FISH to compare chromosome structure in wild-type and DCC-defective embryos (DC mutants), we show that the DCC remodels X chromosomes of hermaphrodites into a spatial conformation distinct from autosomes. The dosage-compensated X chromosomes are composed of Topologically Associating Domains (TADs) that have sharper boundaries and more regular spacing than TADs on autosomes. Most TAD boundaries on X coincide with the highest-affinity rex sites, and these boundaries are lost or diminished in DC mutants, thereby restoring the topology of X to a native conformation resembling that of autosomes. Although most rex sites engage in multiple strong DCC-dependent long-range interactions, the strongest interactions occur between rex sites at the DCC-dependent TAD boundaries. We propose the DCC actively shapes the topology of the entire X chromosome by forming new TAD boundaries and reinforcing pre-existing weak TAD boundaries through interactions between its highest affinity sites. Such changes in higher-order X-chromosome structure then influence gene expression over long distances.
Overall design Our goal was to determine the molecular topology of the dosage compensated X chromosomes of C. elegans. To do so we performed Hi-C analysis and FISH analysis in wild-type XX embryos and mutant XX embryos in which the dosage compensation complex was defective and could therefore not bind to the X chromosome. We showed the dosage compensation complex actively shapes the topology of the entire X chromosome and creates a unique, sex-specific Xconformation that differs from the conformation of autosomes. RNA-seq experiments in wild-type and mutant embryos permitted a comparison between changes in chromosome structure and changes in gene expression.
Contributor(s) Crane E, Bian Q, McCord RP, Lajoie BR, Wheeler BS, Ralston EJ, Uzawa S, Dekker J, Meyer BJ
Citation(s) 26030525
Submission date Nov 28, 2014
Last update date May 15, 2019
Contact name Barbara J. Meyer
Phone 510 643 5583
Organization name HHMI/UCB
Department MCB
Lab Meyer
Street address 16 Barker Hall #3204
City Berkeley
State/province CA
ZIP/Postal code 94720
Country USA
Platforms (1)
GPL18245 Illumina HiSeq 2500 (Caenorhabditis elegans)
Samples (2)
GSM1556154 Wild-Type (N2) Sample
GSM1556155 DC Mutant (SRy93) Sample
This SubSeries is part of SuperSeries:
GSE59716 Condensin-Driven Remodeling of X-Chromosome Topology during Dosage Compensation
BioProject PRJNA268850
SRA SRP050343

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE63717_HiC_libraries_Info.xls.gz 9.2 Kb (ftp)(http) XLS
GSE63717_RAW.tar 89.6 Mb (http)(custom) TAR (of TAR)
GSE63717_SRy93-N2-DpnII-zScoreDifference.tar.gz 21.9 Mb (ftp)(http) TAR
SRA Run SelectorHelp
Raw data are available in SRA
Processed data provided as supplementary file

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